39. Diabetic hyperosmolar syndrome (HHS) and coma

HHS?

Hyperosmolar hyperglycemic state

- Complication that primarily affects elderly people with 2DM

- Can be thought of as the "2DM variant of DKA"

- Is potentially life-threatening - 15% death rate

Symptoms of HHS?

- Vomiting

- Polyuria

- Polydipsia

- Dehydration

- Altered mental state, potentially coma

There is NO ketoacidosis, and therefore NO hyperventilation! (No acidosis)

Development of onset is slow, a few days

HHS can develop due to?

Stress:

- Infections

- Surgeries

- Trauma

- AMI

Incorrect administration of insulin

Cortisol therapy

Why is the blood glucose levels usually higher in HHS than DKA?

DKA symptoms are caused by both hyperglycemia and ketoacidosis, while in HHS there is no ketoacidosis

= This means that the blood glucose level must be higher to produce equally severe symptoms as in DKA

What are the consequences of the slow development of HHS?

Two consequences:

1. Patient has time to realize that something is wrong and can contact help

2. Any decline in mental function may not be easily noticed by others, as it develops so slowly

What people does HHS usually occur in?

Institutionalized, elderly patients who receive poor care and cannot replace fluid themselves

- They also have a reduced feeling of thirst

Pathomechanism of HHS?

Are very similar to those of DKA

Major difference:

- The small amount of insulin present in 2DM patients is enough to prevent lipolysis by inhibiting hormone-sensitive lipase -> preventing ketoacidosis & metabolic acidosis

Hyperglycemia in HHS?

Is more severe in HHS than in DKA

- Osmotic diureses

- Pseudohypoxia

- Hyperosmolarity

- Hypovolemia

is also more severe

Up to 10L of body fluids may be lost!

- These factors cause even stronger non-specific enzyme inhibition than DKA

- Decreased cerebral blood flow due to hypovolemia

- Pseudohypoxia

- Hyperosmolarity increases permeability of the BBB - allowing toxins to cross

HHS and atherosclerosis?

Patients who develop HHS already most likely also have atherosclerosis

- Will further decrease cerebral blood flow

Is there osmotic gap in HHS?

No, as there is no ketone body production

Treatment HHS?

Similar to treatment for DKA

- Except no bicarbonate is needed

Fluid replacement and insulin infusion should be performed very slowly

- K+ should be replaced and all electrolytes should be monitored

Lactic acidosis HHS?

May develop as the hypovolemia causes disordered microcirculation & therefore disordered tissue metabolism

- Much less severe than the DKA

pH may be normal or slightly acidic

Potassium - HHS?

There is a total body-K+ deficit - similar as in DKA

- Insulin deficiency causes K+ to shift out of cells -> which is lost in urine

Coma - HHS?

Develops in 20% of patients

- Occurs when glucose level reaches 60mmol/L

Mechanism is the same as for DKA:

- Decreased cerebral blood flow due to hypovolemia

- Non-specific enzyme inhibition

- Pseudohypoxia

- Hyperosmolarity increases permeability of the BBB - allowing toxins to cross

- Patients w/ HHS usually is also affected by atherosclerosis -> further decreases cerebral blood flow